title: The - 11391 G/A polymorphism of the adiponectin gene promoter is associated with metabolic syndrome traits and the outcome of an energy-restricted diet in obese subjects.
abstract: Adiponectin is an adipose tissue-specific hormone that is commonly decreased in obese subjects. Furthermore, single-nucleotide polymorphisms (SNPs) of the adiponectin gene have been associated with metabolic phenotypes. The present study investigated whether the adiponectin gene promoter variant -11391 G/A (rs17300539) could predict the risk of developing traits characterizing the metabolic syndrome (MetS) and the impact of weight management. The -11391 G/A SNP was genotyped in 180 Spanish volunteers (BMI: 31.4+/-3.2 kg/m (2); age: 35+/-5 years). Clinical measurements were determined at baseline, following an 8-week low-calorie diet (LCD), and at 32 and 60 weeks. At baseline, the GG genotype was associated with higher HOMA-IR, insulin and triacylglyceride concentrations than other genotypes (p<0.05) and was also related with a higher risk of insulin resistance (OR: 2.437, p=0.025) and MetS clinical manifestations (OR: 3.236, p=0.003). Following the LCD, the increased risk in GG subjects compared with others disappeared (p>0.05). By 32 weeks after dietary therapy (n=84), GG carriers had recovered the risk of metabolic comorbidities (OR: 2.420, p=0.043). This risk was even more evident after 60 weeks (OR: 2.875, p=0.014). These data show an increased risk of insulin resistance and MetS complications in obese subjects of the -11391 GG genotype. The risk was markedly reduced during an energy-restricted diet, but was not sustained. Carriage of the A allele therefore confers protection from weight regain, and the effect is particularly evident 32-60 weeks after the dietary intervention, when improvement in GG subjects had disappeared.
authors.affiliation: Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, Pamplona, Spain.
authors.forename: E
authors.initials: E
authors.lastname: Goyenechea
authors.forename: L J
authors.initials: LJ
authors.lastname: Collins
authors.forename: D
authors.initials: D
authors.lastname: Parra
authors.forename: I
authors.initials: I
authors.lastname: Abete
authors.forename: A B
authors.initials: AB
authors.lastname: Crujeiras
authors.forename: S D
authors.initials: SD
authors.lastname: O'Dell
authors.forename: J A
authors.initials: JA
authors.lastname: Martínez
mesh_terms: D052242:Adiponectin / Q000235:genetics; D000328:Adult; D015897:Comorbidity; D004038:Diet, Reducing; D002149:Energy Intake / Q000502:physiology; D005260:Female; D005787:Gene Frequency; D008040:Genetic Linkage; D005838:Genotype; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000453:epidemiology / Q000235:genetics*; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000178:diet therapy* / Q000453:epidemiology / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic; D016896:Treatment Outcome; D015431:Weight Loss / Q000235:genetics
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin